Transdifferentiation of Muscle Satellite Cells to Adipose Cells Using CRISPR/Cas9-Mediated Targeting of MyoD

Chen, Jingjuan; Wang, Chao; Kuang, Shihuan

doi:10.1007/978-1-4939-8897-6_3

Cited by 6 publications

(15 citation statements)

References 38 publications

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“…In addition, inactivation of both MyoD and IGF2 accelerates differentiation of brown preadipocytes and increases the expression of Ucp1 and Prdm16, as well as promotes brown adipose tissue (BAT) development in vivo by increasing Prdm16 expression (Borensztein et al, 2012). At the molecular level, knockout of MyoD drives the transdifferentiation of myoblast via downregulating miR‐133 to activate the PI3K‐Akt signaling pathway and Prdm16 (J. Chen et al, 2019; C. Wang et al, 2017). These findings demonstrate that MyoD acts as a key molecular repressor of the myoblasts to brown adipocytes switching.…”

Section: Factors Inducing Myoblast To Adipocyte Differentiationmentioning

confidence: 99%

“…Moreover, loss of MyoD can facilitate the adipogenic differentiation of myoblasts in vivo (J. Chen et al, 2019;. Conversely, in brown preadipocytes, forced expression of MyoD upregulates the expression of myogenic genes and blocks brown adipogenesis (J.…”

Section: Myodmentioning

confidence: 99%

“…Moreover, loss of MyoD can facilitate the adipogenic differentiation of myoblasts in vivo (J. Chen et al, 2019; C. Wang et al, 2017). Conversely, in brown preadipocytes, forced expression of MyoD upregulates the expression of myogenic genes and blocks brown adipogenesis (J. Chen et al, 2019; C. Wang et al, 2017). Forced expression of MyoD using Adenoviral MyoD vectors stimulates myogenic transdifferentiation in mature adipocytes in vitro and in vivo (Kocaefe et al, 2005).…”

Section: Factors Inducing Myoblast To Adipocyte Differentiationmentioning

confidence: 99%

“…MyoD, one of the MRFs, acts downstream of Myf5 to initiate and control the onset of myogenic differentiation and the formation of skeletal muscle (Rawls et al, 1998; Rudnicki et al, 1993). In C2C12 myoblasts, CRISPR/Cas9‐mediated deletion of MyoD induces their adipogenic transdifferentiation (J. Chen et al, 2019; C. Wang et al, 2017). In primary myoblasts, loss of MyoD promotes brown adipocyte biogenesis and leads to transdifferentiation of myoblasts into brown adipocytes (J. Chen et al, 2019; Wang et al, 2017).…”

Section: Factors Inducing Myoblast To Adipocyte Differentiationmentioning

confidence: 99%

“…In C2C12 myoblasts, CRISPR/Cas9‐mediated deletion of MyoD induces their adipogenic transdifferentiation (J. Chen et al, 2019; C. Wang et al, 2017). In primary myoblasts, loss of MyoD promotes brown adipocyte biogenesis and leads to transdifferentiation of myoblasts into brown adipocytes (J. Chen et al, 2019; Wang et al, 2017). In muscle progenitor cells, MyoD or Myf5 knockdown promotes a cell fate change to brown adipocytes (An et al, 2017; J. Chen et al, 2019).…”

Section: Factors Inducing Myoblast To Adipocyte Differentiationmentioning

confidence: 99%

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Factors inducing transdifferentiation of myoblasts into adipocytes

Wang

Shan

2020

Journal Cellular Physiology

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Fat infiltration in skeletal muscle is observed in several myopathies, is associated with muscular dysfunction, and is strongly correlated with insulin resistance, diabetes, obesity, and aging. In animal production, skeletal muscle fat (also known as intermuscular and intramuscular fat) is positively related to meat quality including tenderness, flavor, and juiciness. Thus, understanding the cell origin and regulation mechanism of skeletal muscle fat infiltration is important for developing therapies against human myopathies as well as for improving meat quality. Notably, age, sarcopenia, oxidative stress, injury, and regeneration can activate adipogenic differentiation potential in myoblasts and affect fat accumulation in skeletal muscle. In addition, several transcriptional and nutritional factors can directly induce transdifferentiation of myoblasts into adipocytes. In this review, we focused on the recent progress in understanding the muscle‐to‐adipocyte differentiation and summarized and discussed the genetic, nutritional, and physiological factors that can induce transdifferentiation of myoblasts into adipocytes. Moreover, the regulatory roles and mechanisms of these factors during the transdifferentiation process were also discussed.

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Section: Factors Inducing Myoblast To Adipocyte Differentiationmentioning

confidence: 99%

Section: Myodmentioning

confidence: 99%

Section: Factors Inducing Myoblast To Adipocyte Differentiationmentioning

confidence: 99%

Section: Factors Inducing Myoblast To Adipocyte Differentiationmentioning

confidence: 99%

Section: Factors Inducing Myoblast To Adipocyte Differentiationmentioning

confidence: 99%

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Factors inducing transdifferentiation of myoblasts into adipocytes

Wang

Shan

2020

Journal Cellular Physiology

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Measurement of GLUT4 Traffic to and from the Cell Surface in Muscle Cells

et al. 2023

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Elevated blood glucose following a meal is cleared by insulin-stimulated glucose entry into muscle and fat cells. The hormone increases the amount of the glucose transporter GLUT4 at the plasma membrane in these tissues at the expense of preformed intracellular pools. In addition, muscle contraction also increases glucose uptake via a gain in GLUT4 at the plasma membrane. Regulation of GLUT4 levels at the cell surface could arise from alterations in the rate of its exocytosis, endocytosis, or both. Hence, methods that can independently measure these traffic parameters for GLUT4 are essential to understanding the mechanism of regulation of membrane traffic of the transporter. Here, we describe cell population-based assays to measure the steady-state levels of GLUT4 at the cell surface, as well as to separately measure the rates of GLUT4 endocytosis and endocytosis.

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Myostatin site‐directed mutation and simultaneous PPARγ site‐directed knockin in bovine genome

Kang

et al. 2020

Journal Cellular Physiology

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Most studies on the acquisition of advantageous traits in transgenic animals only focus on monogenic traits. In practical applications, transgenic animals need to possess multiple advantages. Therefore, multiple genes need to be edited simultaneously. CRISPR/Cas9 technology has been widely used in many research fields. However, few studies on endogenous gene mutation and simultaneous exogenous gene insertion performed via CRISPR/Cas9 technology are available. In this study, the CRISPR/Cas9 technology was used to achieve myostatin (MSTN) point mutation and simultaneous peroxisome proliferator‐activated receptor‐γ (PPARγ) site‐directed knockin in the bovine genome. The feasibility of this gene editing strategy was verified on a myoblast model. The same gene editing strategy was used to construct a mutant myoblast model with MSTN mutation and simultaneous PPARγ knockin. Quantitative reverse‐transcription polymerase chain reaction, immunofluorescence staining, and western blot analyses were used to detect the expression levels of MSTN and PPARγ in the mutant myoblast. Results showed that this strategy can inhibit the expression of MSTN and promote the expression of PPARγ. The cell counting kit‐8 cell proliferation analysis, 5‐ethynyl‐2′‐deoxyuridine cell proliferation analysis, myotube fusion index statistics, oil red O staining, and triglyceride content detection revealed that the proliferation, myogenic differentiation, and adipogenic transdifferentiation abilities of the mutant myoblasts were higher than those of the wild myoblasts. Finally, transgenic bovine embryos were obtained via somatic cell nuclear transfer. This study provides a breeding material and technical strategy to breed high‐quality bovine and a gene editing method to realize the mutation of endogenous genes and simultaneous insertion of exogenous genes in genomes.

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Transdifferentiation of Muscle Satellite Cells to Adipose Cells Using CRISPR/Cas9-Mediated Targeting of MyoD

Cited by 6 publications

References 38 publications

Factors inducing transdifferentiation of myoblasts into adipocytes

Factors inducing transdifferentiation of myoblasts into adipocytes

Measurement of GLUT4 Traffic to and from the Cell Surface in Muscle Cells

Myostatin site‐directed mutation and simultaneous PPARγ site‐directed knockin in bovine genome

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